• 제목/요약/키워드: $3{\beta},\

검색결과 12,119건 처리시간 0.048초

Inhibitory Effects of Quercetin on Muscle-type of Nicotinic Acetylcholine Receptor-Mediated Ion Currents Expressed in Xenopus Oocytes

  • Lee, Byung-Hwan;Shin, Tae-Joon;Hwang, Sung-Hee;Choi, Sun-Hye;Kang, Ji-Yeon;Kim, Hyeon-Joong;Park, Chan-Woo;Lee, Soo-Han;Nah, Seung-Yeol
    • The Korean Journal of Physiology and Pharmacology
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    • 제15권4호
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    • pp.195-201
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    • 2011
  • The flavonoid quercetin is a low molecular weight compound generally found in apple, gingko, tomato, onion and other red-colored fruits and vegetables. Like other flavonoids, quercetin has diverse pharmacological actions. However, relatively little is known about the influence of quercetin effects in the regulation of ligand-gated ion channels. Previously, we reported that quercetin regulates subsets of nicotinic acetylcholine receptors such as ${\alpha}3{\beta}4$, ${\alpha}7$ and ${\alpha}9{\alpha}10$. Presently, we investigated the effects of quercetin on muscle-type of nicotinic acetylcholine receptor channel activity expressed in Xenopus oocytes after injection of cRNA encoding human fetal or adult muscle-type of nicotinic acetylcholine receptor subunits. Acetylcholine treatment elicited an inward peak current ($I_{ACh}$) in oocytes expressing both muscle-type of nicotinic acetylcholine receptors and co-treatment of quercetin with acetylcholine inhibited $I_{ACh}$. Pre-treatment of quercetin further inhibited $I_{ACh}$ in oocytes expressing adult and fetal muscle-type nicotinic acetylcholine receptors. The inhibition of $I_{ACh}$ by quercetin was reversible and concentration-dependent. The $IC_{50}$ of quercetin was $18.9{\pm}1.2{\mu}M$ in oocytes expressing adult muscle-type nicotinic acetylcholine receptor. The inhibition of $I_{ACh}$ by quercetin was voltage-independent and non-competitive. These results indicate that quercetin might regulate human muscle-type nicotinic acetylcholine receptor channel activity and that quercetin-mediated regulation of muscle-type nicotinic acetylcholine receptor might be coupled to regulation of neuromuscular junction activity.

비정규분포공정에서 매디안특수관리도의 모형설계와 적용연구 (Median Control Chart for Nonnormally Distributed Processes)

  • 신용백
    • 기술사
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    • 제20권3호
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    • pp.15-25
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    • 1987
  • Statistical control charts are useful tools to monitor and control the manufacturing processes and are widely used in most Korean industries. Many Korean companies, however, do not always obtain desired results from the traditional control charts by Shewhart such as the X-chart, X-chart, X-chart, etc. This is partly because the quality charterstics of the process are not distributed normally but are skewed due to the intermittent production, small lot size, etc. In Shewhart X-chart, which is the most widely used one in Korea, such skewed distributions make the plots to be inclined below or above the central line or outside the control limits although no assignable causes can be found. To overcome such shortcomings in nonnormally distributed processes, a distribution-free type of confidence interval can be used, which should be based on order statistics. This thesis is concerned with the design of control chart based on a sample median which is easy to use in practical situation and therefore properties for nonnormal distributions may be easily analyzed. Control limits and central lines are given for tile more famous nonnormal distributions, such as Gamma, Beta, Lognormal, Weibull, Pareto, Truncated-normal distributions. Robustness of the proposed median control chart is compared with that of the X-chart, the former tends to be superior to the latter as the probability distribution of the process becomes more skewed. The average run length to detect the assignable cause is also compared when the process has a Normal or a Gamma distribution for which the properties of X are easy to verify, the proposed chart is slightly worse than the X-chart for the normally distributed product but much better for Gamma-distributed products. Average Run Lengths of the other distributions are also computed. To use the proposed control chart, the probability distribution of the process should be known or estimated. If it is not possible, the results of comparison of the robustness force us to use the proposed median control chart based on a normal distribution. To estimate the distribution of the process, Sturge's formula is used to graph the histogram and the method of probability plotting, $X^2$-goodness of fit test and Kolmogorov-Smirnov test, are discussed with real case examples. A comparison of the propose4 median chart and the X chart was also performed with these examples and the median chart turned out to be superior to the X-chart.

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Ascorbic acid extends replicative life span of human embryonic fibroblast by reducing DNA and mitochondrial damages

  • Hwang, Won-Sang;Park, Seong-Hoon;Kim, Hyun-Seok;Kang, Hong-Jun;Kim, Min-Ju;Oh, Soo-Jin;Park, Jae-Bong;Kim, Jae-Bong;Kim, Sung-Chan;Lee, Jae-Yong
    • Nutrition Research and Practice
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    • 제1권2호
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    • pp.105-112
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    • 2007
  • Ascorbic acid has been reported to extend replicative life span of human embryonic fibroblast (HEF). Since the detailed molecular mechanism of this phenomenon has not been investigated, we attempted to elucidate. Continuous treatment of HEF cells with ascorbic acid at ($200{\mu}M$) from 40 population doubling (PD) increased maximum PD numbers by 18% and lowered $SA-{\beta}-gal$ positive staining, an aging marker, by 2.3 folds, indicating that ascorbic acid extends replicative life span of HEF cells. Ascorbic acid treatment lowered DCFH by about 7 folds and Rho123 by about 70%, suggesting that ascorbic acid dramatically decreased ROS formation. Ascorbic acid also increased aconitase activity, a marker of mitochondrial aging, by 41%, indicating that ascorbic acid treatment restores age-related decline of mitochondrial function. Cell cycle analysis by flow cytometry revealed that ascorbic acid treatment decreased G1 population up to 12%. Further western blot analysis showed that ascorbic acid treatment decreased levels of p53, phospho-p53 at ser 15, and p21, indicating that ascorbic acid relieved senescence-related G1 arrest. Analysis of AP (apurinic/apyrimidinic) sites showed that ascorbic acid treatment decreased AP site formation by 35%. We also tested the effect of hydrogen peroxide treatment, as an additional oxidative stress. Continuous treatment of $20{\mu}M$ of hydrogen peroxide from PD 40 of HEF cells resulted in premature senescence due to increased ROS level, and increased AP sites. Taken together, the results suggest that ascorbic acid extends replicative life span of HEF cells by reducing mitochondrial and DNA damages through lowering cellular ROS.

Clostridium 종을 이용한 미역으로부터 아세톤, 부탄올, 에탄올 (ABE) 생산 (Acetone, Butanol, Ethanol Production from Undaria pinnatifida Using Clostridium sp.)

  • 권정은;곽승희;김진아;류지아;박상언;백윤서;허아정;김성구
    • 한국미생물·생명공학회지
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    • 제45권3호
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    • pp.236-242
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    • 2017
  • 본 연구에서는 미역을 이용하여 초고온 열산 가수분해, 효소 당화, 발효과정을 거쳐 아세톤, 부탄올, 에탄올을 생성하는 실험에 대해 진행하였다. 초고온 열산 가수분해에서의 최적 조건은 10%의 slurry, 270 mM의 황산, $160^{\circ}C$에서의 7.5분이었다. 초고온 열산 가수분해는 열처리 시간을 줄이고 적은 농도의 황산을 사용해도 더 많은 당과 적은 저해물질을 생성해 낸다는 장점이 있다. 효소 당화에서는 Viscozyme L (${\beta}-glucanase$, Novozymes)을 12 unit/ml으로 처리하는 것이 25.1 g/l로 가장 많은 단당을 생성했다. 발효에서는 C. acetobutylicum KCTC 1724이 비교적 낮은 pH 5.0에서 많은 아세톤, 부탄올, 에탄올을 생성하는 장점이 있었지만 mannitol을 모두 소비하지 못하는 단점이 있어 고농도의 mannitol 배지에 순치한 C. acetobutylicum KCTC 1724을 사용하여 발효를 진행하였다. 그 결과, 아세톤, 부탄올, 에탄올이 각각 0.99 g/l, 5.62 g/l, 2.44 g/l로 순치하지 않은 C. acetobutylicum KCTC 1724를 이용해 발효했을 때 보다 부탄올은 2.45 g/l, 에탄올은 1.10 g/l 증가했으며 수율($Y_{ABE}$)은 0.24에서 0.37로 증가했다.

당뇨 쥐의 신장 염증 단계에서 단기간의 혼합 항산화 영양소 보충 식이가 산화적 스트레스와 염증반응의 조절에 미치는 영향 (Effects of Short Term Antioxidant Cocktail Supplementation on the Oxidative Stress and Inflammatory Response of Renal Inflammation in Diabetic Mice)

  • 박슬기;박나영;임윤숙
    • Journal of Nutrition and Health
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    • 제42권8호
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    • pp.673-681
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    • 2009
  • Diabetes mellitus is a multifactorial disease. Particularly, diabetic nephropathy is a serious complication for diabetic patients, yet the precise mechanisms that underline the initial stage of diabetic renal inflammation remain unknown. However, oxidative stress induced by hyperglycemia in diabetes is implicated in diabetic renal disease. We hypothesized that dietary supplementation of antioxidants either VCE (0.5% VC + 0.5% VE) or Comb (0.5% VC + 0.5% VE + 2.5% N-acetylcysteine) improves acute diabetic renal inflammation through modulation of blood glucose levels and antioxidant and anti-inflammatory responses. Experimental animals (5.5 weeks old female ICR) used were treated with alloxan (180 mg/kg) once. When fasting blood glucose levels were higher than 250 mg/dL, mice were divided into 3 groups fed different levels of antioxidant supplementation, DM (diabetic mice fed AIN 93G purified rodent diet); VCE (diabetic mice fed 0.5% vitamin C and 0.5% vitamin E supplemented diet); Comb (diabetic mice fed 0.5% vitamin C, 0.5% vitamin E and 2.5% N-acetylcysteine supplemented diet), for 10 days and then sacrificed. Body weights were measured once a week and blood glucose levels were monitored twice a week. Lipid peroxidation products, thiobarbituric acid reacting substances were measured in kidney. NF-${\kappa}B$ activation was indirectly demonstrated by pI${\kappa}B$-${\alpna}$ and expressions of selective inflammatory and oxidative stress markers including antioxidant enzymes were also determined. Dietary antioxidant supplementation improved levels of blood glucose as well as kidney lipid peroxi-dation. Dietary antioxidant supplementation improved NF-${\kappa}B$ activation and protein expression of HO-1, but not mRNA expression levels in diabetic mice fed Comb diet. In contrast, the mRNA and protein expression of CuZnSOD was decreased in diabetic mice fed Comb diet. However, antioxidant supplementation did not improve mRNA and protein expressions of IL-$1{\beta}$ and MnSOD in diabetic mice. These findings demonstrate that acute diabetic renal inflammation was associated with altered inflammatory and antioxidant responses and suggest that antioxidant cocktail supplementation may have beneficial effects on early stage of diabetic nephropathy through modulation of blood glucose levels and antioxidant enzyme expressions.

Induces Vasodilatation of Rat Mesenteric Artery in vitro Mainly by Inhibiting Receptor-Mediated $Ca^{2+}$ -Influx and $Ca^{2+}$ -Release

  • Cao Yong-Xiao;Zheng Jian-Pu;He Jian-Yu;Li Jie;Xu Cang-Bao;Edvinsson Lars
    • Archives of Pharmacal Research
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    • 제28권6호
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    • pp.709-715
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    • 2005
  • The purpose of this study was to investigate the effect of atropine on peripheral vasodilation and the mechanisms involved. The isometric tension of rat mesenteric artery rings was recorded in vitro on a myograph. The results showed that atropine, at concentrations greater than 1$\mu$M, relaxed the noradrenalin (NA)-precontracted rat mesenteric artery in a concentration-dependent manner. Atropine-induced vasodilatation was mediated, in part, by an endothelium-dependent mechanism, to which endothelium-derived hyperpolarizing factor may contribute. Atropine was able to shift the NA-induced concentration-response curve to the right, in a non-parallel manner, suggesting the mechanism of atropine was not mediated via the ${\alpha}_1$-adrenoreceptor. The $\beta$-adrenoreceptor and ATP sensitive potassium channel, a voltage dependent calcium channel, were not involved in the vasodilatation. However, atropine inhibited the contraction derived from NA and $CaCl_2$ in $Ca^{2+}$-free medium, in a concentration dependent manner, indicating the vasodilatation was related to the inhibition of extracellular $Ca^{2+}$ influx through the receptor-operated calcium channels and intracellular $Ca^{2+}$ release from the $Ca^{2+}$ store. Atropine had no effect on the caffeine-induced contraction in the artery segments, indicating the inhibition of intracellular $Ca^{2+}$ release as a result of atropine most likely occurs via the IP3 pathway rather than the ryanodine receptors. Our results suggest that atropine-induced vasodilatation is mainly from artery smooth muscle cells due to inhibition of the receptor-mediated $Ca^{2+}$-influx and $Ca^{2+}$-release, and partly from the endothelium mediated by EDHF.

고지방 식이로 유도된 비만 쥐에서 HPJ 추출물의 항비만 효과 (Anti-Obese Activity of HPJ Extract on High Fat Diet-Induced Obese Mice)

  • 원해단;권해연;장아;김성집;신대희;임방호;정성현
    • 약학회지
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    • 제53권5호
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    • pp.286-292
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    • 2009
  • In this study, we investigated the anti-obese activity of HPJ extract in C57BL/6J mice. The C57BL/6J mice were randomly divided into five groups: normal control group (Con), high fat diet control group (HFD), treatment groups with HPJ at 125 mg/kg (HPJ125), 250 mg/kg (HPJ250), or 500 mg/kg (HPJ500). To induce an obesity, mice were fed by a high fat diet for 6 weeks, and mice were administered with HPJ extract once a day for 8 weeks. At the end of treatment, we examined the effect of HPJ extract on body weight, plasma lipid, and lipogenic enzymes. HPJ extract was found to lower whole body and epididymal adipose tissue weights and lowered plasma levels of glucose, insulin, triglyceride (TG), total cholesterol (TC), non-esterified fatty acid (NEFA) and leptin, compared to those in HFD group. Histological analyses of the liver and fat tissues of mice treated with HPJ extract revealed significantly decreased number of lipid droplets and decreased size of adipocytes compared to the HFD group. In addition, HPJ extract preserved the morphological integrity of pancreatic islets. To elucidate an action mechanism of HPJ extract, Western blot and RT-PCR were performed using epididymal adipose tissues. HPJ extract up-regulated the levels of phosphorylated adenosine monophosphate-activated protein kinase (AMPK) and its substrate, acetyl-CoA carboxylasse (ACC). HPJ extract also attenuated lipogenic gene expressions of sterol regulatory element-binding protein $1{\alpha}$ (SREBP$1{\alpha}$), fatty acid synthase (FAS), sterol-CoA desaturase 1 (SCD1) and glycerol-3-phosphate acyltransferase (GPAT) in dose-dependent manners. In contrast, expressions of lipolytic genes such as peroxisome proliferator-activated receptor-$\alpha$ (PPAR-${\alpha}$) and CD36, and fatty acid $\beta$-oxidation gene, carnitine palmitoyltransferase-1 (CPT-1) were increased. These results suggest that HPJ extract ameliorates obesity through inhibiting synthesis of lipogenic enzymes as well as stimulating fatty acid oxidation resulting from activation of AMPK, and HPJ extract could be developed as a potential therapeutic agent for obese patients.

Korean Red Ginseng alleviates dehydroepiandrosterone-induced polycystic ovarian syndrome in rats via its antiinflammatory and antioxidant activities

  • Choi, Jong Hee;Jang, Minhee;Kim, Eun-Jeong;Lee, Min Jung;Park, Kyoung Sun;Kim, Seung-Hyun;In, Jun-Gyo;Kwak, Yi-Seong;Park, Dae-Hun;Cho, Seung-Sik;Nah, Seung-Yeol;Cho, Ik-Hyun;Bae, Chun-Sik
    • Journal of Ginseng Research
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    • 제44권6호
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    • pp.790-798
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    • 2020
  • Background: Beneficial effects of Korean Red Ginseng (KRG) on polycystic ovarian syndrome (PCOS) remains unclear. Methods: We examined whether pretreatment (daily from 2 hours before PCOS induction) with KRG extract in water (KRGE; 75 and 150 mg/kg/day, p.o.) could exert a favorable effect in a dehydroepian-drosterone (DHEA)-induced PCOS rat model. Results: Pretreatment with KRGE significantly inhibited the elevation of body and ovary weights, the increase in number and size of ovarian cysts, and the elevation of serum testosterone and estradiol levels induced by DHEA. Pretreatment with KRGE also inhibited macrophage infiltration and enhanced mRNA expression levels of chemokines [interleukin (IL)-8, monocyte chemoattractant protein-1), proinflammatory cytokines (IL-1β, IL-6), and inducible nitric oxide synthase in ovaries induced by DHEA. It also prevented the reduction in mRNA expression of growth factors (epidermal growth factor, transforming growth factor-beta (EGF, TGF-β)) related to inhibition of the nuclear factor kappa-light-chain-enhancer of activated B cell pathway and stimulation of the nuclear factor erythroid-derived 2-related factor 2 pathway. Interestingly, KRGE or representative ginsenosides (Rb1, Rg1, and Rg3(s)) inhibited the activity of inflammatory enzymes cyclooxygenase-2 and iNOS, cytosolic p-IκB, and nuclear p-nuclear factor kappa-light-chain-enhancer of activated B in lipopolysaccharide-induced RAW264.7 cells, whereas they increased nuclear factor erythroid-derived 2-related factor 2 nuclear translocation. Conclusion: These results provide that KRGE could prevent DHEA-induced PCOS via antiinflammatory and antioxidant activities. Thus, KRGE may be used in preventive and therapeutic strategies for PCOS-like symptoms.

New Boron Compound, Silicon Boride Ceramics for Capturing Thermal Neutrons (Possibility of the material application for nuclear power generation)

  • Matsushita, Jun-ichi
    • 한국재료학회:학술대회논문집
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    • 한국재료학회 2011년도 춘계학술발표대회
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    • pp.15-15
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    • 2011
  • As you know, boron compounds, borax ($Na_2B_4O_5(OH)_4{\cdot}8H_2O$) etc. were known thousands of years ago. As for natural boron, it has two naturally occurring and stable isotopes, boron 11 ($^{11}B$) and boron 10 ($^{10}B$). The neutron absorption $^{10}B$ is included about 19~20% with 80~81% $^{11}B$. Boron is similar to carbon in its capability to form stable covalently bonded molecular networks. The mass difference results in a wide range of ${\beta}$ values between the $^{11}B$ and $^{10}B$. The $^{10}B$ isotope, stable with 5 neutrons is excellent at capturing thermal neutrons. For example, it is possible to decrease a thermal neutron required for the nuclear reaction of uranium 235 ($^{235}U$). If $^{10}B$ absorbs a neutron ($^1n$), it will change to $^7Li+^1{\alpha}$ (${\alpha}$ ray, like $^4He$) with prompt ${\gamma}$ ray from $^{11}B$ $^{11}B$ (equation 1). $$^{10}B+^1n\;{\rightarrow}\;^{11}B\;{\rightarrow}\; prompt \;{\gamma}\;ray (478 keV), \;^7Li+4{\alpha}\;(4He)\;\;\;\;{\cdots}\; (1)$$ If about 1% boron is added to stainless steel, it is known that a neutron shielding effect will be 3 times the boron free steel. Enriched boron or $^{10}B$ is used in both radiation shielding and in boron neutron capture therapy. Then, $^{10}B$ is used for reactivity control and in emergency shutdown systems in nuclear reactors. Furthermore, boron carbide, $B_4C$, is used as the charge of a nuclear fission reaction control rod material and neutron cover material for nuclear reactors. The $B_4C$ powder of natural B composition is used as a charge of a control material of a boiling water reactor (BWR) which occupies commercial power reactors in nuclear power generation. The $B_4C$ sintered body which adjusted $^{10}B$ concentration is used as a charge of a control material of the fast breeder reactor (FBR) currently developed aiming at establishment of a nuclear fuel cycle. In this study for new boron compound, silicon boride ceramics for capturing thermal neutrons, preparation and characterization of both silicon tetraboride ($SiB_4$) and silicon hexaboride ($SiB_6$) and ceramics produced by sintering were investigated in order to determine the suitability of this material for nuclear power generation. The relative density increased with increasing sintering temperature. With a sintering temperature of 1,923 K, a sintered body having a relative density of more than 99% was obtained. The Vickers hardness increased with increasing sintering temperature. The best result was a Vickers hardness of 28 GPa for the $SiB_6$ sintered at 1,923K for 1 h. The high temperature Vickers hardness of the $SiB_6$ sintered body changed from 28 to 12 GPa in the temperature range of room temperature to 1,273 K. The thermal conductivity of the SiB6 sintered body changed from 9.1 to 2.4 W/mK in the range of room temperature to 1,273 K.

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C57BL/6J db/db생쥐에서 여주 (Momordica Charantia)의 항당뇨 효과 (Effect of bitter melon (Momordica Charantia) on anti-diabetic activity in C57BLI/6J db/db mice)

  • 정재황;이상화;허진주;이기남;남상윤;윤영원;정성훈;이영호;이범준
    • 대한수의학회지
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    • 제48권3호
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    • pp.327-336
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    • 2008
  • Many herbal extracts have been reported to have a preventive or therapeutic effect of on diabetes mellitus. Momordica Charantia commonly known as bitter melon or karela has been reported to be a medicinal plant for treating various diseases including cancers and diabetes. The objectives of this study were to investigate anti-diabetic effects of bitter melon (BM) as determined by blood glucose levels, glucose tolerance test (GTT), insulin tolerance test (ITT), insulin and HbA1C activities in serum, serum biochemical and lipid levels, histopathology, immunohistochemistry and AMPK-${\alpha}2$ expression of skeletal muscle in male C57BL/6J db/db mice. There were four experimental groups including vehicle control, BM 10 mg/kg, BM 50 mg/kg, and BM 250 mg/kg. BM at doses of 10, 50, and 250 mg/kg was orally administered to the diabetic mice everyday for 8 weeks. The treatments of BM 10, 50, and 250 mg/kg significantly decreased the blood glucose level in the diabetic mice compared with vehicle control (p < 0.05). The treatments of BM 10 and 50 mg/kg significantly decreased the GTT, ITT and HbA1c levels in the diabetic mice compared with vehicle control (p < 0.05). All BM groups significantly decreased GOT, GPT, BUN, LDL and glucose levels in the diabetic mice compared with the vehicle control mice (p < 0.05). The livers of mice treated with the BM 10, 50, and 250 mg/kg showed a remarkable decrease in the number of lipid droplets compared with the vehicle control. The pancreas of mice treated with the BM 10, 50, and 250 mg/kg showed a remarkable increase in insulin concentration of ${\beta}$-cells compared with the vehicle control. In addition, the treatments of BM 10, 50, and 250 mg/kg actually increased the expression of AMPK-${\alpha}2$ compared with vehicle control. These results suggest that BM has a respectable anti-diabetic effect resulting from inhibition of blood glucose level and lipid level in serum and that consumption of BM may give a benefit for controlling diabetes mellitus in humans.